From: Long-term potentiation in spinal nociceptive pathways as a novel target for pain therapy
Target, action | Rodent LTP | Human models of secondary hyperalgesia | Human clinical pain | Comments | |
---|---|---|---|---|---|
QST: secondary hyperalgesia | Clinical response: pain report | ||||
Induction (Human postoperative pain) | |||||
μ-opioid receptor agonist | X | X | n.t. (area) X (thr/rating) | controversial | |
NMDA receptor antagonist | X | X 1 | X (area) X (thr/rating) | X | Ketamine also blocks OIH induction in rodents and humans |
α-adrenergic receptor antagonist | X | X | X (area) n.t. (thr/rating) | X | Acute spinal application of clonidine in humans |
NK1 receptor antagonist | X | 0 | n.t. | n.t. | Acute spinal application in rodents vs. chronic oral application in humans |
Modulation of α2δ VGCC subunit | 0 | X/0 | n.t. | X | Acute spinal application in rodents vs. chronic oral application in humans |
Maintenance (Human chronic neuropathic pain) | |||||
μ-opioid receptor agonist | X | X | 0 (area) X (thr/rating) | X | |
NMDA receptor antagonist | 0 | X | X (area) X (thr/rating) | X | |
Modulation of α2δ VGCC Subunit | X | X | n.t. | n.t. | |
α-adrenergic receptor agonist/noradrenaline reuptake inhibitor | X | n.t. | X (area) X (thr/rating) | X | Clonidine (rodents) vs. venlafaxine (humans) |